Biophysical modeling of alpha rhythms during halothane-induced unconsciousness
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Brown_Biophysical modeling.pdf
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Author(s)
Vijayan, Sujith
Ching, ShiNung
Brown, Emery N.
Kopell, Nancy J.
Purdon, Patrick Lee
Date Issued
November 2013
Journal
Proceedings of the 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER)
Publisher
Institute of Electrical and Electronics Engineers (IEEE)
Citation
Vijayan, Sujith, ShiNung Ching, Patrick L. Purdon, Emery N. Brown, and Nancy J. Kopell. “Biophysical Modeling of Alpha Rhythms During Halothane-Induced Unconsciousness.” 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER) (November 2013).
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Author's final manuscript
Abstract
During the induction of general anesthesia there is a shift in power from the posterior regions of the brain to the frontal cortices; this shift in power is called anteriorization. For many anesthetics, a prominent feature of anteriorization is a shift specifically in the alpha band (8-13 Hz) from posterior to frontal cortices. Here we present a biophysical computational model that describes thalamocortical circuit-level dynamics underlying anteriorization of the alpha rhythm in the case of halothane. Halothane potentiates GABA[subscript A] and increases potassium leak conductances. According to our model, an increase in potassium leak conductances hyperpolarizes and silences the high-threshold thalamocortical (HTC) cells, a specialized subset of thalamocortical cells that fire at the alpha frequency at relatively depolarized membrane potentials (>-60 mV) and are thought to be the generators of quiet awake occipital alpha. At the same time the potentiation of GABA[subscript A] imposes an alpha time scale on both the cortical and the thalamic component of the frontal portion of our model. The alpha activity in the frontal component is further strengthened by reciprocal thalamocortical feedback. Thus, we argue that the dual molecular targets of halothane induce the anteriorization of the alpha rhythm by increasing potassium leak conductances, which abolishes occipital alpha, and by potentiating GABA[subscript A], which induces frontal alpha. These results provide a computational modeling formulation for studying highly detailed biophysical mechanisms of anesthetic action in silico.
MIT Department
Massachusetts Institute of Technology. Institute for Medical Engineering & Science
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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DOI of Published Version
https://doi.org/10.1109/NER.2013.6696130
